Swine diseases

Atrophic rhinitis: Bordetella bronchiseptica and Pasteurella multocida (primarily type D)

Swine influenza: influenza virus Mycoplasma pneumoniae: “enzootic

pneumonia,” Actinobacillus pleuropneumoniae: Gram-

negative Pasteurella: Gram negative Verminous pneumonia

Bordatella bronchiseptica◦ aerobic, Gram-negative rod

Pasteurella multocida◦ Gram negative

coccobacillus High ammonia Restricted to swine (described in dog and goat) In the United States, AR is becoming a rare

disease as ◦ early weaning, age

segregation and/or vaccination.

Hx: Described in 1830 and in US in 1944

Clinical signs: 1wk - weaning

early stages: snuffling, sneezing, snorting, ◦ Epiphora, +/- epistaxis

which may progress: atrophy and distortion of the turbinates, nasal and facial bones of some affected pigs

twisted snouts

Dff: rhinitis: porcine reproductive and respiratory syndrome virus (PRRS), pseudorabies virus (PRV), inclusion body rhinitis (cytomegalovirus), or excessive dust or ammonia

Diagnosis Necropsy - 2nd premolar or 1st cheek tooth in pigs

less than 6 months of age Nasal culture for either organism

Toxigenic P. multocida produce a potent toxin that causes a rhinitis with progressive osteopathy of facial and turbinate bones

Treatment tetracyclines in the feed: farrowing/weaning LA200 to neonates

Control or eradicate◦ improvement of husbandry: management and

housing, including ventilation, all in all out, reduce stress

◦ vaccination program for the breeding stock, pigs, or both.

Influenza virus: type A influenza viruses (family Orthomyxoviridae).

Zoonotic Serologic surveys show that nearly

all of the herds in the Midwest have antibodies to SIV

Outbreaks associated with movement or extreme weather changes

up to 100% morbidity low mortality unless secondary

bacterial infection complicates things

Swine influenza subtype H1N1: ◦ 1st appeared in western Illinois in 1918 ◦ influenza pandemic that killed an

estimated 20 million people worldwide

interspecies transmission: among swine, chickens, ducks, turkeys, many wild birds and people

2 or more strains of virus: potential for reassortment (genetic “shift”).

H3N2 and H1N2 emerged during the 1990s: triple reassortment” variants that are comprised of swine, human, and avian viral genes

Both lungs are non-collapsed. There is diffuse tan consolidation of cranial lobes, and multifocal lobular consolidation of the caudal lobes, consistent with bronchointerstitial pneumonia

inflammation with widespread degeneration and necrosis of cells lining bronchi and bronchioles

Sudden: sudden onset of fever, occulonasal discharge, prostration and weakness

Progression: paroxysmal coughing over a relatively short course of 5-7 days

low mortality

Credit: Dr. B. Janke, Iowa State University, College of Veterinary Medicine, Veterinary Diagnostic Laboratory

Diagnosis Necropsy - cranioventral pneumonia:

fluorescent antibody technique on fresh lung sections immunohistochemistry techniques on formalin-fixed lung

sections Treatment - supportive Prevention

closed herd control secondary infections keep away from humans (no shows!)

inactivated by many disinfectants (2 wks environment)

Enzootic pneumonia: acute and severe disease, PRDC (porcine resp dz complex)

Weaned – grower/finisher increases the severity of several other

infections: (PRRS) and influenza Carrier swine very costly, widespread disease of swine,

largely because of its negative effects on growth rate and feed efficiency

Transmission: direct, aerosal, transplacental

Most common cause of chronic pneumonia◦ Chronic, non-productive

cough Low mortality Secondary bacterial

complication Dff

Diagnosis Necropsy - “plum colored”or pale cranio-ventral

pneumonia Culture to rule out secondary bacteriafluorescent antibody, immunohistochemical, or polymerase chain reaction (PCR) techniques

Treatment - Lincomycin in feed

Prevention - improve management

Release toxins

Gram-negative, capsulated, coccobacillary rod

Host specific Intensive swine

operations Inapparent carriers

Peracute, acute, and chronic forms

Clinical signs severe respiratory

distress death

marked dyspnea with mouth breathing +/- bloody discharge from the mouth and nose

Risk factors: ◦ Overstocking, inadequate ventilation, coinfection with

other respiratory pathogen, stress Diagnosis

necropsy - fibrinous pleuropneumonia often diaphragmatic lobes most severe culture is difficult complement fixation serology

Treatment ceftiofur (Naxcel) and procaine penicillin

Control vaccination of young pigs

• Classic lung lesions caused by Actinobacillus pleuropneumoniae.

• Focal areas of necrotizing pneumonia isolated in the dorsal and caudal portions of the lungs is a diagnostic feature.

• the entire lung lobe can also be involved.

• fibrinous pleuritis is common

Gram negative coccobacillus Most common bacterial isolate from pig

lungs opportunistic pathogen

mycoplasma, influenza, actinobacillus, stress clinical signs

moist productive cough dyspnea some die

Diagnosis necropsy - suppurative cranio-ventral

bronchopneumonia may be pleuritis similar to actinobacillus culture

Treatment - penicillin, tetracyclines Control

look for underlying disease medicate feed and water (tetracyclines)

Ascaris suum - direct life cycle◦ pneumonia, hepatitis, and ill thrift

Metastrongylus elongatus - earthworm intermediate Problem with pasture pigs Clinical signs

poor doer respiratory distress

Secondary bacterial infection “Milk spots” liver, worms in the GI Levamisole, ivermectin

• 15-40 cm long, thick bodied, round worms

• Eggs persist in environment 15 yrs

Stomach Ulcers

Small intestine E. coli (piglets): Gram-negative, flagellated bacilli TGE (piglets): coronavirus Clostridium (piglets): large, anaerobic, Gram positive

bacillus Coccidiosis (>7 days): protozoa Rota virus (post weaning) Salmonella (any): Gram-negative bacilli

Large intestine Swine dysentery (grower/finishers): Gram-negative,

anaerobic Proliferative enteropathy (grower/finishers)

Hemorrhagic bowel syndrome Proliferative illeitis

Whipworms (growers) Salmonella (any): Gram-negative bacilli

Infection with and/or agent Unweanedpiglets Nursery pigs Grow/finish pigs Adults

Enterotoxigenic E. coli ++++ +++ + (early grower)

Rotaviral infection ++++ +++ + (early grower)

Transmissible gastroenteritis virus (TGE) ++++ +++ +++ +++

Clostridium difficile ++++

Clostridium perfringens Type A ++++

Clostridium perfringens Type C ++++ + (rare)

CoccidiosisIsospora suis ++++ ++ +

Salmonellosis + ++ ++++ +

Swine dysenteryBrachyspira hyodysenteriae + ++ ++++ ++

Proliferative enteropathiesLawsonia intracellularis ++ ++++ ++

Porcine epidemic diarrhea virus (exotic) +++ +++ ++++ ++++

Whipworm infectionTrichuris suis ++ ++++ +++

Almost always the pars esophagea (non-glandular stomach)

Non-specific lesions Can lead to “bleed-out” Predisposing factors...

Finely ground feed Stress Vit E/Selenium def

Weaning onwards

Melena, ulceration of squamous portion of stomach, anorexia

E. coli: Gram-negative, flagellated bacilli Most impt cause of diarrhea in piglets <5

days old!!! O157:H7, does not appear

to cause disease in swine Toxins Clinical signs

clear watery to pasty brown feces dehydration and depression death losses higher in younger pigs

Diagnosis ph of feces (>8) culture of organism (large number) necropsy - dilated gas filled small intestine

Treatment Ampicillin, tetracyclin, gentamicin, fluids

Control sanitation, vaccination of sow

Coronavirus (similar to FIP) Epidemic form (all ages) Endemic form (1-8 weeks old) WINTER disease Clinical signs

Neonates (1-8 days)– watery diarrhea with undigested milk, vomiting and high mortality rates in piglets

Growers, finishers - diarrhea recovers <7days Morbidity and mortality high in pigs <2weeks

old

Diagnosis ELISA, immunoflourescence of gut contents Necropsy

undigested milk in small intestine thin walled, transparent small intestine

Treatment - supportive Control

isolate new additions for 2 weeks, keep dogs and bird away (carriers)

Immunization of sows or piglets Grind up piglet guts and feed to pregnant sows

Distended intestine with fluid ingesta thin translucent intestinal wall

Clostridium perfringens type C sudden death in 1-2 day old piglets Clinical signs

BLOODY DIARRHEA Diagnosis

Necropsy - blood in jejunum with flecks of mucosa, necrosis of small intestine

Clinical signs Histopathology - large gram positive rods

Treatment usually die too quickly type C antitoxin

Control Sanitation Type C antitoxin within minutes of birth Vaccination of sow Prophylactic bacitracin or penicillin to piglets

http://www.aphis.usda.gov/animal_health/animal_dis_spec/swine/

http://www.ncsu.edu/project/swine_extension/ncporkconf/2002/roberts.htm

http://www.vetmed.wisc.edu/pbs/zoonoses/Erysipelas/erysipelasindex.html

http://vetmed.iastate.edu/vdpam/new-vdpam-employees/food-supply-veterinary-medicine/swine/swine-diseases/haemophilus-parasuis-

http://vetpath.wordpress.com/category/necropsy-cases/

http://www.fmv.utl.pt/atlas/figado/pages_us/figad015_ing.htm

http://www.cfsph.iastate.edu/DiseaseInfo/disease.php?name=influenza&lang=en

http://microgen.ouhsc.edu/a_pleuro/a_pleuro_home.htm